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Chronic renal disease and hypertension are strongly associated with vascular damage, endothelial dysfunction (ED) and increased vascular stiffness. We hypothesized that several novel biomarkers that are more sensitive may be related to relationships between vascular stiffness and reactivity and kidney damage in patients with hypertension.

Design and method:

Urine levels of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver fatty-acid binding protein (L-FABP) and serum levels of Cystatin C and creatinine were measured by quantitative enzyme immunoassay in 92 hypertensive patients, divided into four age and sex-matched groups according to severity of hypertension: 1 grade (n=24), 2 grade (n = 26), 3 grade (n = 17) and resistant hypertension (n = 25). Glomerular filtration rate (GFR) was estimated by MDRD and CKD-EPI formulas. Instrumental examination was performed after 5 days of discontinuation of antihypertensive medications including applanation tonometry (SphygmoCor, Artcor Medical) with the calculation of central aortic pressure, pulse wave velocity (PWV) and augmentation index (AI). Endothelial function was assessed by reactive hyperemia index (RHI) with EndoPAT device (Itamar Medicals).


Patients with resistant hypertension were characterized by higher Cystatin C (0.97 +/- 0.18 pg/ml; p = 0.01) and L-FABP (9270.2 +/- 30394.5 pg/ml; p = 0.05), while there were no differences in creatinine, eGFR, NGAL and KIM-1 levels between groups. Novel biomarkers levels were associated with increased arterial stiffness in resistant population: L-FABP levels with PWV (r = 0.470, p = 0.0001), Cystatin C with PWV (r = 0.251, p = 0.03) and NGAL grades - with AI (r = 0.314, p = 0.005). No correlation was between RHI and biomarkers of renal damage, besides RHI remained within normal values in all patients (more than 1.67).


NGAL, Cystatin C and L-FABP seem to be associated with increased arterial stiffness but not with ED in patients with severe, resistant to treatment hypertension.

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